Celiac disease (also known as celiac sprue, non-tropical sprue or gluten-sensitive enteropathy) is a common autoimmune condition triggered by ingesting wheat proteins called gluten. In cereal grains and flour, such as wheat, rye or barley, gluten is a complex mixture of proteins including alcohol-soluble monomers called gliadins and alcohol-insoluble polymers called glutenins. Gliadins can be divided into alpha, gamma and omega types on the basis of their amino acid sequences and mobility on electrophoresis. The glutenin subunits can be divided into high molecular weight (HMG) and low molecular weight (LMG) groups.
The clinical spectrum of gluten sensitivity includes typical celiac disease associated with the classical features of fatigue, chronic diarrhoea, malabsorption of nutrients, weight loss, abdominal distension, anemia, as well as a failure to thrive in young children.
The typical form of celiac disease has an incidence of approximately 1 in 2500 in people of European descent, and also occurs in North African and Asian populations in lower incidence. The atypical form is also found in those who have latent onset of the disease. In total, the incidence of typical and atypical forms is about 1 in 1500. Asymptomatic celiacs are discovered when relatives of celiacs are tested. Latent celiacs are defined as those who have one of the companion diseases such as other autoimmune disorders such as diabetes, arthritis, Sjogren's syndrome, thyroid disease, collagen vascular disease, and liver disease. When combined, these various presentations of celiac disease reach as high as 1 in 300.
In celiac patients, gluten triggers an auto-immune attack. The ingested gluten carries epitopes capable of activating T cells, so the process can be considered to be an autoimmune disease. There are two major components leading to the disease: a genetic background and environmental factors that will trigger the disease to a full expression of typical or atypical symptoms.
The large majority of celiac patients express human leukocyte antigen HLA-DQ2 or DQ8 molecules, or both. Enterocytes, cells on the lining of the small intestine, have receptors which are ‘programmed’ by the Class II antigens to recognize gluten. The gluten binds to HLA receptors that are present on the enterocytes. When this binding occurs, there is a migration to the other side of the cells. This receptor-gluten complex can reach cells in the bloodstream. There are lymphocytes that are responsible for the production of toxic compounds that are ultimately responsible for tissue damage in the intestine. Among them, T helper I cells and cytokines apparently play a major role in a local inflammatory process and also stimulate B-cells differentiation in plasma cells producing antibodies.
Currently, the only acceptable treatment for celiac disease is strict adherence to a 100% gluten-free diet for life. An adherence to a gluten-free diet can prevent almost all complications caused by the disease. A gluten-free diet means avoiding all products that contain wheat, rye and barley, or any of their derivatives, for example in commercial soups, sauces, ice creams, hot dogs, and other foods.
However, this is a difficult task as there are many hidden sources of gluten found in the ingredients of many processed foods. Many commercial products, ready meals and convenience foods are made with wheat flour, gluten-containing wheat proteins or gluten-containing starches added as a filler, stabilizing agent or processing aid. These include sausages, fish fingers, cheese spreads, soups sauces, mixed seasonings, mincemeat for mince pies, and some medications and vitamin supplements. Another possible source of contamination of gluten-free products occurs when they are produced using the same production lines and equipment employed for making gluten-containing foods.
In view of the serious and widespread nature of celiac disease, natural methods of treating or ameliorating the effects of the disease are needed. The present invention is directed to addressing such a need.